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35 publications mentioning rno-mir-140

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-140. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 205
By binding Smad3 mRNA 3′-untranslated region (3′-UTR), miR-140 can downregulate Smad3 expression directly [4], [5]. [score:9]
In summary, our results demonstrate that low-dose PTX prevents EMT transition and ameliorates pulmonary fibrosis by upregulating miR-140 expression to further suppress the TGF-β1/Smad3 pathway, which highlighted a new way for pulmonary fibrosis therapy. [score:8]
These results induced by miR-140 are similar to those affected by PTX treatment, which indicates miR-140 participates in the antifibrotic process by downregulating the expression of Smad3 and prevents its subsequent phosphorylation in AECs. [score:6]
Then, we asked whether upregulation of miR-140 could suppress TGF-β1/Smad3 activities to further affect EMT in AECs. [score:6]
PTX suppressing TGF-β1 pathway by upregulation of miR-140. [score:6]
This study provides the evidence of an important role of low-dose PTX in ameliorating EMT and pulmonary fibrosis by upregulating miR-140 to suppress the activities of TGF-β1/Smad3 pathway. [score:6]
The above results demonstrate the miR-140 expression is negatively related to TGF-β1 activities, and miR-140 levels in the TGF-β1-stimulated A549 cells and BLM -induced rat lungs were dramatically upregulated by PTX treatment (** P<0.05, Figure 1 D, E and 2 D). [score:6]
These results confirm that miR-140 downregulates Smad3 expression by binding to Smad3-3′ UTR in AECs. [score:6]
Our results showed that the TGF-β1 activity could be suppressed by PTX, which promotes us to examine the effect of PTX on miR-140 expression. [score:5]
Recent studies confirm that the TGF-β1 pathway is suppressed by miR-140 through targeting Smad3 in the C3H10T1/2 and 3T3 cell lines [4], [5]. [score:5]
MiR-140 expression is downregulated in low grade liver fibrosis [61]. [score:5]
We also found that overexpression of miR-140, same as PTX treatment, could reverse TGF-β1 -induced EMT in A549 cells by increasing the E-cadherin level and decreasing the expression of vimentin, Smad3 and p-Smad3. [score:5]
Moreover, our results reveal that miR-140 overexpression increases the sensitivity of AECs to PTX, but more precise mechanisms of cooperation of PTX and miR-140 in suppressing TGF-β1/Smad3 -induced pulmonary fibrosis need further study. [score:5]
To further verify the roles of miR-140 and PTX in TGF-β1/Smad3 pathway, we studied whether overexpression of miR-140 would have similar effects as PTX on fibrosis-related protein expression. [score:5]
E-cadherin expression was increased and vimentin was downregulated obviously in miR-140- or PTX+miR-140 -treated cells, especially in PTX+miR-140 -treated cultures, compared to TGF-β1- or TGF-β1+D-NC -treated controls. [score:5]
The miR-140 level in BLM-instilled rat lungs reached its nadir on 7 d, approximately two folds lower than that in untreated or sham control lung tissues, while it was dramatically upregulated in PTX -treated lung tissues. [score:4]
Effect of PTX on upregulating miR-140. [score:4]
Moreover, PTX could block the action of TGF-β1 by upregulating miR-140. [score:4]
Our results revealed that miR-140 is downregulated in BLM -induced pulmonary fibrosis, which is negatively related with TGF-β1 activities. [score:4]
MiR-140 can suppress the TGF-β1 pathway through targeting Smad3 in the C3H10T1/2 and 3T3 cell lines [4], [5]. [score:4]
Our results demonstrated that low-dose PTX reversed the TGF-β1 -induced EMT in A549 cells as well as RLE-6TN cells, and improved the BLM-instilled pulmonary fibrosis in rat lungs with miR-140 upregulation and Smad3/p-Smad3 diminishment. [score:4]
PTX ameliorates EMT and upregulates miR-140 in A549 cells. [score:4]
These reports imply that downregulation of miR-140 would promote pulmonary fibrosis. [score:4]
Cells treated with both TGF-β1 and miR-140, in part, appeared elongated morphology to cobblestone-like morphology transition, and the levels of Smad3 and p-Smad3 were downregulated in these cells (Figure 6 A, B). [score:4]
Our results showed that miR-140 overexpression led to a notable reduction in the expressions of fibrosis-related proteins (TGF-β1, vimentin, Smad3 and p-Smad3) compared to the NC controls (* P<0.05, Figure 4C), which was supported by other studies [31], [40], while these proteins levels were increased concomitant with a stellate and elongated fibroblast-like morphology after ASO-140 treatment (** P<0.05, Figure 4A, C). [score:4]
These results suggested that the downregulation of miR-140 might be an important event in fibrotic responses. [score:4]
The levels of vimentin, Smad3 and p-Smad3 levels were increased and E-cadherin was downregulated in TGF-β1 -treated A549 cells, which were reversed in PTX-, or PTX+miR-140 -treated cells, especially in both PTX and miR-140 -treated cultures. [score:4]
Regulation of miR-140 to EMT-related gene expression. [score:4]
Similarly, we found that there was a notable reduced expression of miR-140 during TGF-β1 -treated EMT in A549 cells, BLM -induced pulmonary fibrosis in rat lungs and lung samples of IPF patients. [score:3]
E: miR-140 expression in human pulmonary fibrotic lungs. [score:3]
The miR-140 expression was significantly reduced in TGF-β1 treated A549 cells, while was increased dramatically after PTX treatment (Fig. 1 D, E). [score:3]
E: Quantitative RT-PCR analysis of miR-140 expression. [score:3]
MiR-140 can negatively regulate the expression of Smad3 [4], [5], which acts as a key factor in TGF-β1 -mediated EMT [32] and the fibrosis response [30]– [32], [57]. [score:3]
In Fig. 4 A, B, GFP expression and the number of GFP -positive cells in miR-140 -treated cultures were much lower than those in D-NC- or ASO-140 -treated controls. [score:3]
To further confirm the effect of PTX on suppressing TGF-β1/Smad3 activities through miR-140, we investigated whether miR-140 overexpression would amplify the actions of PTX. [score:3]
Smad3 has been found to be a target for miR-140 in a pluripotent mouse embryonic fibroblast cell line [4], [5]. [score:3]
Moreover, both miR-140 and PTX treatment resulted in a better reversal of the TGF-β1 -induced E-cadherin and vimentin expression (Figure 7 A–C). [score:3]
GFP-Smad3 plasmid (containing Smad3 mRNA 3′-UTR targeted by miR-140) was constructed to transfect A549 cells with miR-140. [score:3]
MiR-140, D-NC (miR-140 mutation control with mutation seed sequences), ASO-140 (specific to miR-140 sequence) and S-NC (the single-stranded RNA negative control) were cooperated with pcDNA-GFP-UTR vector, respectively, to transfect A549 cells using Lipofectamine 2000 transfection reagent (Invitrogen, USA) according to the manufacturer's instructions. [score:3]
MiR-140 expression was normalized against U6 and other regulated genes were normalized with GAPDH. [score:3]
In A549 cells, the miR-140 expression was significantly reduced after TGF-β1 treatment compared with untreated controls, but it was obviously increased after additional interference with TGF-β1 signal pathway blocker SB431542 (* P<0.05, Figure 1 D, E), suggesting that miR-140 correlated inversely with TGF-β1 activities. [score:2]
MiR-140 affected EMT and Smad3/p-Smad3 expression. [score:2]
However, the miR-140 expression was restored to higher level with PTX treatment compared to only BLM -treated rats (** P<0.05, Figure 2 D). [score:2]
The miR-140 treatment led to an obvious reduction in the expression of TGF-β1, vimentin, Smad3 and p-Smad3 compared to the D-NC control groups. [score:2]
Control, cells untreated with miRNA or plasmid; GFP-Smad3, cells treated with pcDNA-GFP-UTR; D-NC, cells treated with both D-NC (miR-140 mutation control) and pcDNA-GFP-UTR plasmid; S-NC, cells treated with both S-NC (the single-stranded RNA control) and pcDNA-GFP-UTR; miR-140, cells treated with both miRNA-140 and pcDNA-GFP-UTR; ASO-140, cells treated with both ASO-140 and pcDNA-GFP-UTR. [score:2]
D: MiR-140 expression is determined by RT-PCR. [score:2]
Moreover, PTX treatment dramatically increased the miR-140 expression compared to TGF-β1 -treated cells, and slightly lower than that in untreated cells (** P<0.05, Figure 1 D, E). [score:2]
PTX ameliorates pulmonary fibrosis andu pregulates miR-140 in fibrotic lungs. [score:2]
MiR-140 suppresses the TGF-β1/Smad3 pathway in A549 cells. [score:2]
MiR-140 suppressing TGF-β1/Smad3 pathway. [score:2]
However, the role of miR-140-related TGF-β1/Smad3 pathway in pulmonary fibrogenesis remains unclear. [score:1]
If miR-140 is a major leader to prevent pulmonary fibrosis, it may either precede or coincide with the synthesis of TGF-β1 [62]. [score:1]
In the lung tissues of BLM -treated rats, the miR-140 levels reached their nadir on day 7, approximately two-fold lower than that of in the untreated controls. [score:1]
A549 cells treated with TGF-β1 or TGF-β1+ D-NC underwent a fibroblast-like morphology, while their morphologies were reversed by miR-140 or miR-140 plus PTX treatment. [score:1]
A gradually increase of miR-140 level was observed with BLM-exposed time extension, between 21 d and 28 d with no more substantial changes, but still much lower than that in untreated or sham controls (* P<0.05, Figure 2 D, the 21 d data not shown). [score:1]
Treatment with both miR-140 and PTX would lead to a cobblestone-like epithelial morphology and the lowest levels of Smad3/p-Smad3 in TGF-β1 -treated cells (Figure 6 A, B). [score:1]
TGF-β1 was added into miR-140- or ASO-140 -transfected A549 cells for 24 h prior to PTX (50 nM) treatment. [score:1]
Furthermore, their morphologies and these protein levels became more close to those in both miR-140 and PTX treatment cells (Figure 5 A, B). [score:1]
Together, these results support that miR-140 increases the efficiency and sensitivity of the reversal effect of PTX on EMT. [score:1]
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2
[+] score: 74
They also observed that miR-140 could suppress the expression of Mfn1 and that it exerted its effect on mitochondrial fission and apoptosis through Mfn1 targeting [30]. [score:7]
Interestingly, as shown in Fig.   3, at 4 weeks post-MI, with the exception of miR-143-3p, changes in miR-30a-5p, miR-30c-5p, miR-145-5p, and miR-140-3p expression tended to increase compared to the control group, whereas the expression of these four miRNAs decreased and the expression of miR-143-3p increased in the SkM +MI group, suggesting that these miRNAs may be associated with SkM therapy in myocardial injury. [score:6]
With the exception of miR-143-3p, we observed that changes in the expression of miR-30a-5p, miR-30c-5p, miR-145-5p, and miR-140-3p at 4 weeks post-MI tended to increase compared to the control group, whereas expression of these four miRNAs decreased and the expression of miR-143-3p increased in the SkM treatment group, suggesting that these miRNAs could be associated with the SkM therapy of myocardial injury. [score:6]
We observed a significant trend in the expression of some apoptosis-related miRNA and mRNA, including the expression of miR-30a-5p, miR-30c-5p, miR-145-5p, miR-143-3p, and miR-140-3p (Fig.   3). [score:5]
GO-Analysis based on miRNA targeted genes showed significant function of target genes by rno-miR-30a-5p, rno-miR-30c-5p, rno-miR-140-3p, rno-miR-143-3p, and rno-miR-145-5p. [score:5]
We focused on changes in some apoptosis -associated miRNA and in gene expression in response to SkM MI therapy, corroborated some of the results obtained from microarrays with real-time qPCR analysis, and selected some significant miRNAs, including miR-30a-5p, miR-30c-5p, miR-145-5p, miR-143-3p, and miR-140-3p, which were involved with anti-apoptotic target genes such as Angptl4, Dpep1, Egr1, Eif5a, Tsc22d3, Irs2 and Cebpb. [score:5]
Pathway analysis based on miRNA targeted genes showed significant pathways targeted by rno-miR-30a-5p, rno-miR-30c-5p, rno-miR-140-3p, rno-miR-143-3p, and rno-miR-145-5p. [score:5]
We focused on a novel set of apoptosis -associated miRNAs and their target genes, among which 4 miRNAs (miR-30a-5p, miR-30c-5p, miR-145-5p, miR-140-3p), except one (miR-143-3p), were downregulated in the SkM treated group as compared to the untreated group. [score:5]
We also demonstrated that miR-140, miR-143 and miR-145 might also collectively cooperate in MI treatment with SkMs by regulating targeted genes such as Egr1. [score:4]
MicroRNA-GO-Network, screening out the main function of the target genes regulated by rno-miR-30a-5p, rno-miR-30c-5p, rno-miR-140-3p, rno-miR-143-3p, and rno-miR-145-5p. [score:4]
Venn’s diagram for target genes of rno-miR-30a-5p, rno-miR-30c-5p, rno-miR-140-3p, rno-miR-143-3p, and rno-miR-145-5p predicted by MIRANDA, MICROCOSM, MIRDB. [score:3]
MIRANDA, MICROCOSM, and MIRDB programs were employed to predict potential targets of five key miRNAs, miR-30a-5p, miR-30c-5p, miR-145-5p, miR-143-3p, and miR-140-3p. [score:3]
Our data also suggest that some apoptosis -associated miRNAs, such as miR-30a-5p, miR-30c-5p, miR-145-5p, miR-143-3p, miR-140-3p and their target genes, may play an important role in myocardial injury after MI. [score:3]
We focused on five apoptosis-related miRNAs (miR-30a-5p, miR-30c-5p, miR-145-5p, miR-143-3p, and miR-140-3p), demonstrated their changes after SkMs treatment and filtered out 7 anti-apoptotic target genes, namely, Angpt14, Eif5a, Egr1, Irs2, Cebpb, Tsc22d3, and Dpep1, in the heart tissues (Fig.   6). [score:3]
In this experiment, we focused on a subset of apoptosis-related miRNAs, including miR-30a-5p, miR-30c-5p, miR-145-5p, miR-143-3p, and miR-140-3p, and mRNAs involved in anti-apoptotic target genes such as Angptl4, Dpep1, Egr1, Eif5a, Tsc22d3, Irs2 and Cebpb. [score:3]
A study demonstrated that knockdown of miR-140 was able to reduce myocardial infarct sizes in an animal mo del. [score:2]
The five key miRNAs in the network were identified as miR-30a-5p, miR-30c-5p, miR-145-5p, miR-143-3p, and miR-140-3p. [score:1]
In this study, we selected four apoptosis-related genes to be assayed by RT-PCR, including Angptl4, Dpep1, Eif5a, and Tsc22d3, which are regulated by miR-140-3p. [score:1]
The five key miRNAs in the network were identified as miR-30a-5p, miR-30c-5p, miR-145-5p, miR-143-3p, and miR-140-3p, as shown in Additional file 12: Figure S4. [score:1]
The expression of miR-30a-5p, miR-30c-5p, miR-145-5p, miR-143-3p, and miR-140-3p in the infarcted border zone region was measured by real-time analysis 4 weeks after MI. [score:1]
The results from real-time qPCR analysis showed high concordance with our microarray results for all investigated transcripts, as shown in Fig.   4. Fig.  4 Analyses of the expression of rno-miR-30a-5p, rno-miR-30c-5p, rno-miR-140-3p, rno-miR-143-3p, and rno-miR-145-5p by RT-PCR. [score:1]
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3
[+] score: 55
This biphasic pattern is opposite to the monophasic expression pattern of miR-140-3p and observed in our study where the expression levels peaked in the repair phase (Fig.   2a, c), indicating that miR-140-3p and may suppress the expression of TNF-α and IL-1a, respectively, in the repair phase. [score:9]
They identified Dnpep as a miR-140-5p target gene whose up-regulation plays a causal role in the skeletal defects of MiR-140 -null mice by reducing BMP signaling. [score:6]
There were significant differences between days 3 and 7, 7 and 10, 10 and 14, 14 and 21, and 21 and 28 in the expression of miR-140-3p (p < 0.05), whereas there were significant differences between days 7 and 10, 10 and 14, 14 and 21, and 21 and 28 in the expression of miR-140-5p (p < 0.05). [score:5]
This study identified, for the first time, that five miRNAs, miR-140-3p, miR-140-5p,,, and, are highly expressed with dynamic expression patterns in standard healing fractures in rats. [score:5]
Fig. 3Expression of miR-140-3p (a), miR-140-5p (b), (c), (d), and (e) in standard healing fractures (solid bars) and in unhealing fractures (blank bars) on post-fracture days 3 and 7, as analyzed by real-time PCR. [score:3]
a, p < 0.05 versus values on day 3 in standard healing fracture; b, p < 0.05 versus values on day 7 in standard healing fracture; c, p < 0.05 versus values on day 10 in standard healing fracture; d, p < 0.05 versus values on day 21 in standard healing fracture; e, p < 0.05 versus values on day 28 in standard healing fracture The expression of miR-140-3p and-5p was significantly higher in standard healing fractures than in unhealing fractures on post-fracture days 7, 10, and 14 (p < 0.05) (Figs.   2a, b and 3a, b). [score:3]
Of the five identified miRNAs, miR-140-5p,,, and have been reported to be involved in the regulation of skeletal development (Table  2). [score:3]
miR-140-5p is abundantly expressed in cartilaginous tissues during embryogenesis and also in adult cartilage [9]. [score:3]
Nakamura et al. demonstrated that miR-140-5p plays an essential role in skeletal development by regulating processes of endochondral ossification [29]. [score:3]
Fig. 2Expression of miR-140-3p (a), miR-140-5p (b), (c), (d), and (e) in standard healing fractures (solid bars) and in unhealing fractures (blank bars) on post-fracture days 3 and 7, as analyzed by real-time PCR. [score:3]
Collectively, these four miRNAs, namely miR-140-5p,,, and, may play important roles during fracture healing by regulating intramembranous and/or endochondral ossification. [score:2]
Microarray and real-time polymerase chain reaction (PCR) analyses on day 14 revealed that five miRNAs, miR-140-3p, miR-140-5p,,, and, were significantly highly expressed in standard healing fractures compared with unhealing fractures. [score:2]
Taken together, miR-140-3p,, and may play important roles during fracture healing via the regulation of inflammation. [score:2]
Of the five identified miRNAs, miR-140-3p,, and have been reported to be involved in the regulation of inflammatory responses (Table  2). [score:2]
With these criteria we identified eight miRNAs: miR-140-3p, miR-140-5p,,, miR-208b-3p,, miR-743b-5p, and miR-879-3p (Table  1). [score:1]
miR-140-3p and miR-140-5p. [score:1]
The five miRNAs, miR-140-3p, miR-140-5p,,, and, identified using microarray and real-time PCR analyses may play important roles during fracture healing. [score:1]
These miRNAs were miR-140-3p, miR-140-5p,,, and. [score:1]
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4
[+] score: 24
Diminution of circulating miR-140 might be the result of an upregulated TGF-β signaling pathway during disease progression. [score:6]
Zhang X. Chang A. Li Y. Gao Y. Wang H. Ma Z. Li X. Wang B. miR-140-5p regulates adipocyte differentiation by targeting transforming growth factor-β signaling Sci. [score:4]
Adipocyte differentiation is regulated by miR-140 via targeting the TGF-β signaling pathway. [score:4]
The blood level of miR-140 was more than 12-fold suppressed at late-stage diabetes (Figure 5). [score:3]
Decreased miR-140 levels are associated with impaired regulation of osteogenesis and adipogenesis [46]. [score:2]
Diminution in circulating levels was detected for miR-140, miR-151-3p, miR-185, miR-203, miR-434-3p and miR-450a (Figure 5). [score:1]
At late-stage diabetes, the circulating level of 12 miRNAs was specifically altered; the circulating level of miR-375, miR-210 and miR-133a was increased, and the circulating levels of let-7i, miR-140, miR-450a, miR-185, miR-186, miR-151-3p, miR-203, miR-16 and miR-685 were strongly diminished versus their levels at the pre-diabetes stage (Figure 4). [score:1]
Metformin leads to decreased circulating miR-140-5p (miR-140) and miR-122 levels in T2D patients [62]. [score:1]
The decrease of miR-140 at initial hyperglycemia might correlate with the dysfunctional adipocytes in ZDF rats and the insulin resistance of ZDF rat adipocytes [47]. [score:1]
The strongest diminished miRNA in blood was miR-140, reaching an approximately 12-fold reduction at late-stage diabetes. [score:1]
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5
[+] score: 18
miR-140 expression is significantly decreased in human OA chondrocytes [16], thus favoring an increased expression of its target genes and consequently a role in cartilage degradation. [score:7]
Targeted deletion of miR-140 in mice resulted in age-related OA-like changes [17]. [score:3]
Of importance, miR-140 decreases the expression of genes known to play detrimental roles in OA cartilage. [score:3]
Miyaki S. Nakasa T. Otsuki S. Grogan S. P. Higashiyama R. Inoue A. Kato Y. Sato T. Lotz M. K. Asahara H. MicroRNA-140 is expressed in differentiated human articular chondrocytes and modulates interleukin-1 responses Arthritis Rheum. [score:2]
miR-140, which was originally found in cartilage, has been linked more specifically to OA [15, 16]. [score:1]
Miyaki S. Sato T. Inoue A. Otsuki S. Ito Y. Yokoyama S. Kato Y. Takemoto F. Nakasa T. Yamashita S. MicroRNA-140 plays dual roles in both cartilage development and homeostasis Genes Dev. [score:1]
Furthermore, more and more individual miRNAs, including miR-27b, miR-34a, miR-140, and miR-146a, have been linked to arthritis pathogenesis [6, 13, 14]. [score:1]
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6
[+] score: 14
Several miRNAs are demonstrated that associated with OA development and modulation such as miR-18a (chondrocyte differentiation), miR-27b (controlling the expression of MMP-13), miR-34a (prevention of cartilage degradation), miR-140 and miR-222 (controlling cartilage homeostasis), miR-146 (promotion of inflammatory OA), miR146a (OA cartilage pathogenesis), miR-675 (cartilage repair) [30, 31]. [score:4]
It have been reported that miR-140 is specifically expressed in cartilage tissue to activate or supress PDGF, SOX9, Sp1, aggrecan, VEGF and HDAC4 [28, 41]. [score:3]
The level of expressed miRNAs of interest, rno-miR-199a-3p, rno-miR-181a-5p, rno-miR-140-3p and rno-miR-27b-3p, were confirmed by quantitative RT-PCR in articular cartilage and subchondral bone (Figure 5A and 5B). [score:3]
Several miRNAs including miR-140, miR-199a, mir-193 and mir-29a/29b control the anabolic and catabolic regulation in cartilage [42]. [score:2]
The rno-miR-199a-3p, rno-miR-181a-5p, rno-miR-140-3p and rno-miR-27b-3p were measured from articular cartilage A. and subchondral bone B. The expression profiles of each miRNA matched the tested probes at least three times repeat. [score:1]
Figure 5The rno-miR-199a-3p, rno-miR-181a-5p, rno-miR-140-3p and rno-miR-27b-3p were measured from articular cartilage A. and subchondral bone B. The expression profiles of each miRNA matched the tested probes at least three times repeat. [score:1]
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7
[+] score: 11
In the mo del group, 17 miRNAs were downregulated, including miR-1, miR-133, miR-29, miR-126, miR-212, miR-499, miR-322, miR-378, and miR-30 family members, whereas the other 18 miRNAs were upregulated, including miR-21, miR-195, miR-155, miR-320, miR-125, miR-199, miR-214, miR-324, and miR-140 family members. [score:7]
Among these differentially expressed miRNAs, miR-1, miR-133, miR-29, miR-126, miR-499, miR-30, miR-21, miR-195, miR-155, miR-199, miR-214, and miR-140 have been reported to be related to MI [25– 36], while the other miRNAs have not been reported directly in MI. [score:4]
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8
[+] score: 10
For example, rno-miR-1-3p, rno-let-7 family, rno-miR-29a-3p, rno-miR-133a-3p, rno-miR-499-5p and rno-miR-140-3p are most highly expressed in both HF and control group in our study, which was consistent with the previous studies that rno-miR-133, rno-miR-1 and rno-miR-499 are highly expressed in the heart[26], and miR-1, let-7 and miR-133 are highly expressed in the murine heart[27]. [score:7]
The most highly expressed miRNAs were rno-miR-1-3p, rno-let-7 family, rno-miR-29a-3p, rno-miR-133a-3p, rno-miR-499-5p and rno-miR-140-3p in both HF and control group. [score:3]
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9
[+] score: 9
Other miRNAs from this paper: hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-107, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-139, hsa-mir-181c, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-15b, hsa-mir-23b, hsa-mir-132, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-154, hsa-mir-186, rno-mir-324, rno-mir-129-2, rno-mir-20a, rno-mir-7a-1, rno-mir-101b, hsa-mir-29c, hsa-mir-296, hsa-mir-30e, hsa-mir-374a, hsa-mir-380, hsa-mir-381, hsa-mir-324, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-15b, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19b-2, rno-mir-19a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-27a, rno-mir-29c-1, rno-mir-30e, rno-mir-30a, rno-mir-30c-2, rno-mir-32, rno-mir-92a-1, rno-mir-92a-2, rno-mir-93, rno-mir-107, rno-mir-129-1, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-146a, rno-mir-154, rno-mir-181c, rno-mir-186, rno-mir-204, rno-mir-212, rno-mir-181a-1, rno-mir-222, rno-mir-296, rno-mir-300, hsa-mir-20b, hsa-mir-431, rno-mir-431, hsa-mir-433, rno-mir-433, hsa-mir-410, hsa-mir-494, hsa-mir-181d, hsa-mir-500a, hsa-mir-505, rno-mir-494, rno-mir-381, rno-mir-409a, rno-mir-374, rno-mir-20b, hsa-mir-551b, hsa-mir-598, hsa-mir-652, hsa-mir-655, rno-mir-505, hsa-mir-300, hsa-mir-874, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-874, rno-mir-17-2, rno-mir-181d, rno-mir-380, rno-mir-410, rno-mir-500, rno-mir-598-1, rno-mir-674, rno-mir-652, rno-mir-551b, hsa-mir-3065, rno-mir-344b-2, rno-mir-3564, rno-mir-3065, rno-mir-1188, rno-mir-3584-1, rno-mir-344b-1, hsa-mir-500b, hsa-mir-374c, rno-mir-29c-2, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Finally, other subsets of miRNAs were either up-regulated (miR-23a-3p, miR132-3p, miR-146a-5p, miR-154-3p, miR-181d-5p, miR-212-3p, miR-212-5p, miR-344b-5p, miR-380-3p, miR-410-3p, miR-433-3p and miR-3584; Fig. 2, Supplementary Fig. S4), or down-regulated (miR-29c-5p, miR-30a-5p, miR-30c-2-3p, miR-30e-3p, miR-138-5p, miR-140-3p, miR-551b-3p and miR-652-3p; Fig. 2, Supplementary Fig. S5) during all phases of the disease. [score:9]
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10
[+] score: 8
Other miRNAs from this paper: rno-mir-16, rno-mir-23b, rno-mir-203a, rno-mir-203b, rno-mir-15a
In avian skeletal muscle, miR-140-3p inhibits MYMK expression and is involved in myotube formation [32], which raises the possibility that PMS-2G11 cells secrete miRNAs that function in the downregulation of MYMK. [score:8]
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11
[+] score: 7
In addition to miR-146a, other miRNAs may also play important roles in OA pathogenesis: miR-140, a cartilage-specific miRNA, regulates gene expression of ADAMTS-5 in chondrocytes [25]; and miR-140 [-/- ]mice display an OA-like phenotype [26]. [score:4]
miR-140 may also be involved in the formation and maintenance of cartilage through targeting HDAC4 [27]. [score:3]
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[+] score: 6
Miyaki, et al. [17] reported that miR-140 could down-regulate ADAMTS-5 expression in IL-1β -induced OA chondrocytes. [score:6]
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[+] score: 6
Serum was collected from different stage at 1 [st] to 6 [th] week and the expression levels of 4 top ranked miRNAs (miR-25-3p, miR-140-5p, miR-342-5p and miR-150-5p) were assayed by qPCR. [score:2]
By geNorm, miR-25-3p was ranked as the most stable gene and a combination of miR-25-3p, miR-342-5p and miR-140-5p was recommended for optimal normalization (Fig. 2a). [score:1]
Therefore, ten miRNAs (miR-19b-3p, miR-21-5p, miR-25-3p, miR-30a-5p, miR-133b-3p, miR-140-5p, miR-150-5p, miR-199a-3p, miR-342-5p, miR-3473) were chosen as candidate reference genes. [score:1]
Conversely, miR-140-5p, miR-342-5p and miR-150-5p were not as stable as miR-25-3p and showed some notable changes at some stage (Fig. 2c). [score:1]
With this algorithm, miR-140-5p was identified as the most stable gene, followed by miR-25-3p (Fig. 2b). [score:1]
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14
[+] score: 6
It was found to be targeted by multiple microRNAs in our analysis, including miR-143, miR-30 family members, miR-140, miR-27b, miR-125a-5p, miR-128ab, and miR-342-3p. [score:3]
Among the important genes were Lifr, Acvr1c, and Pparγ which were found to be targeted by microRNAs in our dataset like miR-143, miR-30, miR-140, miR-27b, miR-125a, miR-128ab, miR-342, miR-26ab, miR-181, miR-150, miR-23ab and miR-425. [score:3]
[1 to 20 of 2 sentences]
15
[+] score: 6
Besides, miR-140, miR-181a-5p and miR-451 expression were all highly increased during fracture healing process [18] and miR-21 overexpression [19] or miR-92a knockdown [20] would enhance fracture healing property. [score:6]
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16
[+] score: 5
Other miRNAs from this paper: rno-mir-21, rno-mir-210
MiR-140 which is specifically expressed in cartilage regulates cartilage development and homeostasis, and its loss contributes to the development of age-related OA-like changes 21. [score:5]
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17
[+] score: 5
miR-140 was also found to act on the target gene HDAC4 to overcome resistance to antitumor drugs [41]. [score:3]
Finally, miR-140 participated in the immune response in the colons of rats with DSS -induced UC. [score:1]
Five of these miRNAs were altered in colon tissues or peripheral blood in previous studies (miR-126, miR-214, miR-532, miR-140, and miR-340). [score:1]
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18
[+] score: 5
In addition, we observed reduced expression of miR-9 and miR-140 expression consistent with that observed on ethanol exposure [44]. [score:5]
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19
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-204, rno-mir-205, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-1, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-31b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-mir-155, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-322-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
For instance, among the 66 uniformly expressed miRNAs for which IPA assigned functions, we identified 12 candidates that have been implicated in androgen regulation, including: let-7a-5p, miR-15a-5p, miR-17-5p, miR-19b-3p, miR-23a-3p, miR-24-3p, miR-27b-3p, miR-30a-5p, miR-34a-5p, miR-140-5p, miR-193a-3p, miR-205-5p (S1 Fig). [score:4]
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[+] score: 4
For example, evidence indicate that let-7, miR-140 and miR-92a are crucial for skeletal development [4– 5]; and deficiency of these miRNAs suppress the proliferation as well as the differentiation of growth plate chondrocytes, leading to a dramatic growth defect [4– 5]. [score:4]
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[+] score: 4
Reports have shown that miR-208 and miR-140 affect their host genes 25, 26; however, miR-26 suppresses its host gene to regulate neurogenesis [27]. [score:4]
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22
[+] score: 4
Other miRNAs from this paper: hsa-mir-140
Liang Y. Duan L. Xiong J. Zhu W. Liu Q. Wang D. Liu W. Li Z. Wang D. E2 regulates MMP-13 via targeting miR-140 in IL-1beta -induced extracellular matrix degradation in human chondrocytes Arthritis Res. [score:4]
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[+] score: 4
Other miRNAs from this paper: rno-mir-101b, rno-mir-27b, rno-mir-34a, rno-mir-101a, rno-mir-199a
MicroRNA-140 is expressed in differentiated human articular chondrocytes and modulates interleukin-1 responses. [score:2]
Many miRNAs, such as miR-140 (ref. [score:1]
Molecular mechanisms of the cartilage-specific microRNA-140 in osteoarthritis. [score:1]
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24
[+] score: 4
MiR-140, a cartilage-specific miRNA, regulates the expression of Adamts-5 in chondrocytes, [23] and miR-140-/- mice display an OA-like phenotype. [score:4]
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25
[+] score: 3
That is, miR-140, miR-31, miR-875-5p and miR-141 were expressed mainly during tooth morphogenesis identified at embryonic day 16 (E16), whereas miR-689, miR-720, miR-711 and miR-455 were prevalent at the cytodifferentiation stage (E18) [8]. [score:3]
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26
[+] score: 3
Wiskott-Aldrich syndrome protein family member 1 (Wasf1), which was found to be regulated by miR-17-5p, miR-93, miR-191, miR-451, miR-146a and miR-140, has been shown to be a protective alcohol-responsive gene in the prefrontal cortex of human alcoholics (38). [score:2]
Among the dysregulated miRNAs, miR-490 exhibited an increment in the ASH and AFL groups, while miR-140, miR-7a, miR-451, miR-93, miR-146a and miR-191 levels exhibited a decline in the ASH and AFL groups compared with the respective controls (Table II). [score:1]
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27
[+] score: 3
In retrospect, such miRNAs as miR-9, miR-27 (Gene ID: 407018), miR-140 (Gene ID: 406932), and miR-146 have been indicated to be abnormally expressed in OA patients. [score:3]
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[+] score: 3
Compared to the other 2 groups, 21 miRNAs are upregulated in 6-hour group as shown in the upper portion of Fig. 2, miR-9, miR-204, miR-335, miR-23a, miR-708, miR-146a, miR-325-5p, miR-106b, miR-143, miR-140, miR-376b-3p, miR-7a, miR-541, miR-185, miR-499, miR-127*, miR-320, miR-140*, miR-145*, miR-423*, miR-378. [score:3]
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[+] score: 2
Li J Mitofusin 1 is negatively regulated by microRNA140 in cardiomyocyte apoptosisMol. [score:1]
Since the subject of our study was IRI, we selected nine miRNAs that have been reported to be involved either in oxidative stress (such as miR-150 and miR-21) 14, 15 or in cardiomyocyte apoptosis (such as miR-195, miR-132, miR-140, miR-144, miR-24, miR-214 and miR-34a) 16– 21 in our investigation and, using quantitative PCR (qPCR), explored whether RIPC could modify the expression level of these nine miRNAs in plasma exosomes. [score:1]
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[+] score: 2
Among the miRNAs that undergo the greatest dynamic regulation at early time points were miR-219 and miR-140 (Figure S1A) and at the later time point were miR-322 and miR-128a (Figure S2B, 3 and 24 h). [score:2]
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31
[+] score: 1
Miyaki S. Sato T. Inoue A. Otsuki S. Ito Y. Yokoyama S. Kato Y. Takemoto F. Nakasa T. Yamashita S. MicroRNA-140 plays dual roles in both cartilage development and homeostasisGenes Dev. [score:1]
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32
[+] score: 1
Miyaki S. Sato T. Inoue A. Otsuki S. Ito Y. Yokoyama S. Kato Y. Takemoto F. Nakasa T. Yamashita S. MicroRNA-140 plays dual roles in both cartilage development and homeostasis Genes Dev. [score:1]
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[+] score: 1
Additionally all reads of sequences originally reported in miRbase as the minor strand (*) were grouped (upon similar criteria as above; Table S5) resulting in a further 58 miRNAs of interest, 16 of which (including miR-126*, miR-140*, miR-151* and miR-28*) were detected between 1.23 and 99.56 fold higher in the * form than the ‘major’ mature sequence, while miR-501* was not detected in the major mature strand form. [score:1]
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34
[+] score: 1
Other miRNAs from this paper: hsa-mir-140
Pando R. Even-Zohar N. Shtaif B. Edry L. Shomron N. Phillip M. Gat-Yablonski G. MicroRNAs in the growth plate are responsive to nutritional cues: Association between miR-140 and SIRT1J. [score:1]
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[+] score: 1
For example, miR-105, miR-125b and miR-140 are involved in the inflammatory phase; miR-15a, miR-15b and miR-16 participate in the granulation phase; and miR-29 and miR-192 function in the remo deling phase [10]. [score:1]
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